The study of defective repair of MNNG (N-methyl-N'-nitro-N-nitrosoguanidine) produced damage was extended. One fifth (14/70) of the human tumor cell strains tested comprises a group of cell strains (Mer minus) that differs from the remaining 56 tumor strains (Mer plus) or from normal human fibroblasts (also Mer plus) in the following ways: 1) Inability to excise O to the 6th power-methylguanine from their DNA after being treated with MNNG; 2) relative inability to support the growth of MNNG damaged adenovirus 5; and 3) sensitivity to being inactivated by MNNG or BCNU (Bis-chloroethyl-nitrosurea) in a reproductive way. The results may be relevant to uncovering the molecular reasons for success of certain bifunctional alkylating chemotherapeutic agents (BCNU, CCNU).